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首页> 外文期刊>Cytokine >Gamma delta (γδ) T-cells are critical in the up-regulation of inducible nitric oxide synthase at the burn wound site
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Gamma delta (γδ) T-cells are critical in the up-regulation of inducible nitric oxide synthase at the burn wound site

机译：γδT细胞在烧伤创面上诱导型一氧化氮合酶的上调中至关重要

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Background: The high incidence of morbidity and mortality following major burn can in part be attributed to immune derangements and wound healing complications. Inflammation plays an important role in wound healing, of which inducible nitric oxide synthase (iNOS) derived nitric oxide is a central mediator. T-cells of the γδ TCR lineage have also been shown to be important in healing of the burn wound site. Nonetheless, the role of γδ T-cells in the regulation of the burn wound iNOS expression is unknown. Methods: Wildtype (WT) and δ TCR -/- male C57BL/6 mice were subjected to burn (3rd degree, 12.5% TBSA) or sham treatment. Three days after injury, skin samples from non-injured and the burn wound were collected and analyzed for the expression of iNOS and cytokines and chemokine levels. In a second series of experiments, WT mice were subjected to burn and left untreated or treated with the iNOS inhibitor, L-Nil. Skin cytokine and chemokine levels were assessed 3days thereafter. Results: Burn induced an 18-fold increase in iNOS expression at the wound site as compared to the uninjured skin of WT sham mice. In δ TCR -/- mice iNOS expression at the wound site was significantly lower than that of the WT group. Burn also induced increased levels of IL-1β, IL-6, G-CSF, TNF-α, KC, MCP-1, MIP-1α and MIP-1β at the wound site in WT and δ TCR -/- mice, but G-CSF, TNF-α, and MIP-1β levels were greater in δ TCR -/- mice. Inhibition of iNOS activity in WT mice with L-Nil suppressed burn wound levels of IL-1β, G-CSF, and MIP-1α, whereas IL-6, TNF-α, KC, MCP-1 and MIP-1β were unaffected. Conclusions: T-cells of the γδ TCR lineage significantly contribute to the up-regulation of iNOS expression which contributes to wound inflammation.
机译：背景：大面积烧伤后高发病率和高死亡率的部分原因可归因于免疫紊乱和伤口愈合并发症。炎症在伤口愈合中起着重要作用，其中诱导型一氧化氮合酶（iNOS）衍生的一氧化氮是主要的介质。 γδTCR谱系的T细胞在烧伤创面愈合中也很重要。尽管如此，尚不清楚γδT细胞在烧伤创面iNOS表达调控中的作用。方法：对野生型（WT）和δTCR-/-雄性C57BL / 6小鼠进行烧伤（3度，12.5％TBSA）或假处理。受伤三天后，收集未受伤和烧伤创面的皮肤样品，分析iNOS和细胞因子的表达以及趋化因子水平。在第二系列实验中，WT小鼠被烧伤，未经治疗或以iNOS抑制剂L-Nil治疗。此后3天评估皮肤细胞因子和趋化因子水平。结果：与野生型WT假小鼠的皮肤相比，烧伤在伤口部位诱导的iNOS表达增加了18倍。在δTCR-/-小鼠中，伤口部位的iNOS表达明显低于WT组。烧伤还诱导了WT和δTCR-/-小鼠伤口部位的IL-1β，IL-6，G-CSF，TNF-α，KC，MCP-1，MIP-1α和MIP-1β水平升高，但是δTCR-/-小鼠的G-CSF，TNF-α和MIP-1β水平较高。用L-Nil抑制WT小鼠的iNOS活性可抑制烧伤创面的IL-1β，G-CSF和MIP-1α水平，而IL-6，TNF-α，KC，MCP-1和MIP-1β不受影响。结论：γδTCR谱系的T细胞显着促进iNOS表达的上调，这有助于伤口发炎。

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